Myocardial infarction (MI), resulting mainly from atherosclerosis, remains a leading cause of morbidity and mortality worldwide [1-2]. Atherosclerosis is a multifaceted, asymptotic, and complicated disease. While the exact mechanisms of atherogenic factors are not currently known, current laboratory screening tests focus on the profile of circulating lipids and lipoproteins to gauge cardiovascular risk. A large lipid burden, in particular elevated levels of LDL cholesterol, represent a significant risk for atherosclerosis. However, a large number of studies suggest that atherosclerosis is a chronic immune-inflammatory disease and lipid burden alone is not a sufficient factor to accurately predict cardiovascular risk.
Monocytes are intimately linked to the early phases of the inflammatory response and the interaction of monocytes with activated luminal endothelium is a key step leading to atherosclerosis[3]. Monocytes mediated by chemotactic factors, jump and roll along the endothelial monolayer [4] until integrin, once activated on the surface of monocyte, strongly combines with vascular endothelial cells. Therefore, the level of integrin activated on the monocyte surface is an important index to evaluate the risk of artery atheromatous plaque formation and the subsequent risk for myocardial infarction. Current screening tests do not consider the role of integrin expression and monocytes in the pathogenesis of the disease.